An ICD is a medical device for implant within a patient that recognizes various arrhythmias such as ventricular tachycardia (VT) and ventricular fibrillation (VF) and selectively delivers electrical shocks to terminate the arrhythmia. Prior to delivering therapy, it is important to distinguish a tachycardia arising in the ventricles from one arising elsewhere in the heart. A tachycardia arising in the ventricles (referred to as VT) is often more serious than a tachycardia arising elsewhere in the heart since VT can sometimes lead to VF, which can be fatal if untreated. In contrast, a supraventricular (SVT) is a tachyarrhythmia whose origin is above the ventricles but which is conducted to the ventricles resulting in unacceptably rapid ventricular rate. The true underlying arrhythmia of SVT may be, e.g., atrial fibrillation (AF), sinus tachycardia (ST), ectopic atrial tachycardia, atrial reentry tachycardia, atrioventricular (AV) nodal reentry tachycardia, paroxysmal AF or atrial flutter. Failure to distinguish SVT from VT can result in delivery of inappropriate therapy. Depending upon the capabilities of the ICD, inappropriate therapy might involve delivery of unnecessary and painful electrical shocks to the heart or improper delivery of anti-tachycardia pacing (ATP.) Misidentification of SVT and VT is one of the leading causes of improper device therapy.
Accordingly, it is desirable to efficiently and reliably distinguish SVT from VT. Some discrimination techniques used by state-of-the-art ICDs analyze the morphology of a ventricular intracardiac electrogram (IEGM) to distinguish SVT from VT. The ventricular IEGM is an electrical signal sensed internally by the device, which is associated with the contraction and expansion of the ventricular chambers of the heart. More specifically, the contraction of ventricular muscle tissue is triggered by the depolarization of the ventricles, which is manifest within the ventricular IEGM as an R-wave (also referred to as the “QRS complex.”) Repolarization of the ventricles is manifest as a T-wave in the ventricular IEGM. Note that the contraction of atrial muscle tissue also generates electrical signals. Specifically, the contraction of the atria is triggered by the electrical depolarization of the atria, which is manifest as a P-wave in the IEGM. A similar repolarization of the atrial tissue usually does not result in a detectable signal within the IEGM because it coincides with, and is obscured by, the R-wave. For the purposes of discriminating SVT from VT, the atrial signals are typically ignored and only ventricular signals are examined. (Note that the terms P-wave, R-wave and T-wave may also be used to refer to corresponding features of a surface electrocardiogram (ECG.) Herein, however, these terms are primarily used to refer to features of the IEGM.)
Morphological discrimination of VT and SVT typically exploits the fact that R-waves occurring during a tachycardia of ventricular origin have a different shape from R-waves triggered from normal atrio-ventricular conduction from the atria. This is because the sequence of activation of the ventricular cardiac muscles differs depending on whether the trigger source is within the ventricles (as opposed to via the normal AV conduction mechanism.) Accordingly, morphologic discrimination procedures typically record R-wave morphology during normal sinus rhythm and then generate and save a morphology template based on the sinus rhythm R-wave for use during tachycardia. If a tachycardia is detected (based on the ventricular rate exceeding a VT threshold), the R-waves during the tachycardia are compared against the template. If there is a substantial match, the tachycardia is deemed SVT and no ventricular shock or ATP therapy is delivered. Instead, other forms of therapy might be delivered to address the SVT. On the other hand, if there is no match the tachycardia is deemed to be VT or VF and so ATP therapy or a shock might be delivered. In some devices, if the rate exceeds a higher VF threshold, a defibrillation shock is promptly delivered regardless of waveform morphology under the assumption that the arrhythmia is a potentially fatal VF. See, for example, techniques described in U.S. Pat. No. 7,974,687 to Farazi et al., entitled “Methods and Systems for Enhanced Arrhythmia Discrimination.”
Various waveform discrimination techniques are described in, e.g., U.S. Pat. No. 5,273,049 to Steinhaus et al. entitled, “Detection of Cardiac Arrhythmias using Template Matching by Signature Analysis”; U.S. Pat. No. 5,240,009 to Williams, entitled “Medical Device with Morphology Discrimination”; U.S. Pat. No. 5,779,645 to Olson et al., “System and Method for Waveform Morphology Comparison,” and U.S. Pat. No. 6,516,219 to Street, entitled “Arrhythmia Forecasting based on Morphology Changes in Intracardiac Electrograms.” See, also, the morphological discrimination techniques described in U.S. patent application Ser. No. 11/674,974, filed Feb. 14, 2007 of Graumann, entitled “System and Method for Morphology-Based Arrhythmia Discrimination using Left Ventricular Signals sensed by an Implantable Medical Device.”
Note that during normal sinus rhythm—in particular when the aforementioned template is being generated—a certain amount of variability in R-wave morphology is normal. The variability is caused by a variety of factors, including changes in posture, diurnal variations and other physiological variables. Thus, throughout the day the R-wave will have a central or average morphology but specific R-waves will have varying morphology around this average. Over a longer period there can be other fundamental changes to the central or average R-wave morphology due to effects such as cardiac remodeling, cardiac disease progression, ischemia, etc. For this reason, the morphology template should be periodically updated to reflect the current sinus R-wave morphology. Accordingly, a template update process can be used to periodically record and save the shape of R-waves for use as a template. The time of each template update is based on a clock timer. When the timer expires, a template update process is initiated to generate and record a new template. When the template update process records the new template, a number of rules may be applied to ensure that the complex saved is, in fact, an R-wave rather than a premature ventricular contraction (PVC), noise artifact or some other signal.
Even when such rules are applied, complications can arise due to the variability of R-wave morphology. In particular, at the time of a template update, the R-wave morphology may be near its central value or it may be at an extreme of its variation for the patient or somewhere in-between. Similarly, when a tachycardia occurs, the R-wave morphology may be at or near its central value or it may be at an extreme of its variation for the patient or somewhere in-between. For example, if the template waveform is acquired at one extreme of the R-wave morphology variation and a subsequent SVT occurs at the opposite extreme of the R-wave morphology variation, then the comparison of the template to the tachycardia R-wave will reflect the full extent of the different waveform morphologies. This might result in possible misidentification of the SVT as a VT because the R-waves during SVT might not match the template R-wave, although both are supraventricular in origin. In this regard, the closer the template is to a central value for the R-wave morphology (as opposed to an extreme), the more likely that a correct SVT determination will be made.
Accordingly, it would be desirable to provide improved techniques for updating morphology templates that avoid these and other problems.